Many scientific studies have demonstrated the role played by the intestinal flora in the pathogenesis of chronic rheumatic inflammatory diseases such as rheumatoid arthritis, ankylosing spondylitis or post-infectious rheumatism.
For example, no signs of arthritis are observed in germ-free animals (transgenic rats or mice), whereas their littermates harboring intestinal flora develop signs of arthritis (Rath H C, et al; J. Clin. Invest; 98(4); 945-953; 1996 and Abdollahi-Roodsaz S., et al; J. Clin. Invest; 118; 205-216; 2008).
Moreover, in human beings, studies have shown that patients in whom rheumatoid arthritis was recently diagnosed harbored few bifidobacteria, compared with control subjects (Vaahtovuo J, et al; J. Rheumatol; 35; 690-693; 2008) and, when the equilibrium of the intestinal flora was partially restored by introducing a vegetarian diet, the patient's condition was found to be improved (Peltonen R, et al; J. Rheumatol; 36; 64-68; 1997). Finally, it is well known that the use of certain antibiotics which modify the composition of the intestinal flora improves the signs of rheumatoid arthritis (Stone M. et al.; J. Rheumatol; 30; 2112-2122; 2003).
One of the mechanisms which explains the involvement of the intestinal flora in the pathogenesis of chronic rheumatic diseases lies in its ability to regulate bacterial translocation. The mechanism of bacterial translocation is defined as the crossing of the intestinal barrier by intestinal bacteria. These intestinal bacteria are taken up and then transported by cells of the intestinal immune system, such as dendritic cells or macrophages, to the synovial site, causing a source of painful inflammation of rheumatic type in the joints.
The composition of the intestinal flora has an influence on this process. Thus, when bifidobacteria widely colonize the lower part of the intestine, they show an ability to reduce bacterial translocation (Romond M B, et al.; Anaerobe; 14; 43-48; 2008).
Moreover, the composition of the intestinal flora also has an influence on the expression level of genes involved in the inflammatory response, such as galectins (Romond M B, et al; Fems Immunol Med Microbiol; 55; 85-92; 2009).
There are at the current time many products capable of modifying the intestinal flora, such as prebiotics or probiotics. On the other hand, few of them have a positive impact on bacterial translocation. Among the products which have a beneficial action with respect to bacterial translocation, is the macromolecule isolated from Bifidobacterium breve culture. Indeed, it has been demonstrated, in documents WO 2004/093898 and WO 2006/040485, that the oral administration of this macromolecule leads to a decrease in translocation and in bacterial dissemination, and that the said molecule exhibits a preventive activity against collagen-induced arthritis in mice. However, a residual pro-inflammatory activity is always observed with the use of the macromolecule isolated from Bifidobacterium breve culture, thereby limiting its use in the field of inflammatory diseases.
It would therefore be advantageous to have a product which enables a decrease in bacterial translocation to be obtained and which would not exhibit any residual pro-inflammatory activity.
As it happens, the applicant has discovered that the use of a macromolecular complex isolated from Bifidobacterium longum complex makes it possible to satisfy these requirements.